Hydrocortisone - how to use it safely and without causing adrenal suppression

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Hydrocortisone is a steroid and steroids in high doses have nasty side effects. So how is it safe to use? All my patients, quite rightly, ask this question. The name of the game is the dose. All substances inside the body have a "right dose" from protein and fat to water and minerals. Too much of any one causes problems, as does too little of any one.

The same is true for hormones. Too much causes side effects as does too little. Too much steroid causes immune suppression, high blood pressure, diabetes and osteoporosis. No steroid at all invariably results in death. Too little steroid causes fatigue. The key is to use the right amount.

A normal adrenal gland produces 20-25mgs of hydrocortisone daily. Most of this is in the morning with production tailing off as the day progresses. It is linked in with the internal body clock. When I prescribe cortisol I only do so in patients with a proven deficiency, I use 5-10mgs (rarely 15mgs) to be taken either in the morning, or morning and lunchtime. Levels do not need to be monitored at this low dose.

The safety of low dose cortisone has been long established but the following is an abstract from a recent paper in the Lancet. It shows how low dose cortisol in unselected patients not only improved symptoms in patients with CFS but there was no adrenal suppression at follow up.

Prednisolone may also be used - this is a pro-drug - it is converted n the liver to hydrocortisone. It is more convenient to use because just a once daily dose is needed.

A New Hydrocortisone Trial

A randomised, controlled, crossover trial of low-dose hydrocortisone treatment for CFS has recently been published. 32 participants, fulfilling both the Oxford and CDC 1994 criteria, completed this short-term trial. Participants received 5mg or 10mg of hydrocortisone for 28 days and placebo for 28 days.

The results revealed modest, statistically significant improvements in fatigue with this low-dose hydrocortisone treatment compared with placebo. The degree of disability was also reduced with hydrocortisone treatment but not with placebo. There was no significant difference in changes in fatigue score when 5mg and 10mg doses were compared. The authors suggest that, in view of the lack of dose response in this study, 5mg is a sufficient low of hydrocortisone.

Participants who responded to this hydrocortisone treatment did not differ from 'non-responders' in terms of their pre-treatment cortisol levels. Although none of the participants in this study had a current psychiatric illness, those who responded to hydrocortisone treatment had fewer psychiatric symptoms prior to treatment.

Based on the results of the insulin stress test, this short-term, low dose hydrocortisone treatment was not found to cause significant suppression of adrenal gland function. None of the participants dropped out of the study and only minor side effects were reported.

The authors conclude that this low-dose hydrocortisone treatment resulted in "significant reduction in self-rated fatigue and disability in patients with chronic fatigue syndrome".

This study sheds interesting light on the possible role of low cortisol levels in the disease processes involved in CFS. Caution is required, however, in interpreting the results. Participants' baseline cortisol levels could not predict their response to hydrocortisone treatment and participants appeared to have baseline cortisol levels within the normal reference range.

In another randomised controlled trial of hydrocortisone therapy (see Interaction 29, page 21 for a review), McKenzie at al., used a higher 'low-dose' hydrocortisone treatment of 25 - 35mg daily. They found that this dose was associated with some improvements in symptoms but caused significant adrenal suppression. Neither of these research teams currently recommended the use of hydrocortone as a treatment for CFS. The present study assessed the effects of hydrocortisone treatment in the short-term only. As the authors point out, further studies, involving longer durations of treatment and follow-up are required to assess the long-term effectiveness and safety of this treatment.

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References

  • Cleare et al; The Lancet, 1999, Vol. 353 February 6, p455-458

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